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The Neural Basis of Psychotic-Like Experiences

Student thesis: Doctoral ThesisDoctor of Philosophy

Evangelos Papanastasiou

Objective
Psychotic‐Like Experiences (PLE) are subclinical manifestation of psychotic symptoms and may reflect an increased vulnerability to psychotic disorders. Contemporary models of psychosis propose that dysfunctional reward processing and emotional dysregulation is involved in the aetiology of psychosis.
Objective
To examine the neuroimaging profile of healthy adolescents with an increased presence of PLE, during a face processing and a reward processing task.
Method
1,434 adolescents were assessed at two timepoints using functional MRI during a Faces Task (FT) and a Monetary Incentive Delay (MID) Task at age 14 and 19 years. The sample was stratified into two groups of high PLE and low PLE based on their scores on the CAPE‐42 questionnaire at age 19. The first level analysis focused on a pre‐defined contrast of [Angry Faces] – [Control Stimuli] for the FT and two pre‐defined contrasts of [Anticipation of Large Win] – [Anticipation of No Win] and [Feedback of Large Win] – [Feedback of No Win] for the MID task. The second level analysis examined between‐group differences using an a priori defined region of interest approach (ROIs). I performed a factorial analysis to examine the main effects of group, time and their interaction on brain activation. Additionally, I performed an exploratory analysis, by employing both a cross‐sectional design to compare brain activation levels between the high PLE and low PLE groups at ages 14 and 19, and a longitudinal design to compare brain activation levels between the two timepoints.
Results
FT: Adolescents presenting with elevated overall PLE scores at age 19 years exhibited an early state (BL) of hyperactivation in right insular cortical areas, during perception of angry faces; this was replaced by a later state (FU) of hypoactivation in right prefrontal and right limbic cortical areas and left striatal subcortical areas, during perception of angry faces. There was a decrease in activation of right limbic cortical areas, from BL to FU, in the high general PLE group.
MID: Adolescents presenting with elevated overall PLE scores at age 19 years exhibited an early state (BL) of hypoactivation in left and right prefrontal and left limbic cortical areas, during reward feedback; this was replaced by a later state (FU) of hypoactivation in right striatal subcortical areas, during the reward anticipation. There was also an increase in activation of left and right prefrontal areas, from BL to FU, in the high general PLE group.
Conclusions
The FT results suggest evidence of aberrant changes during adolescent development with reduced limbic and insular activation over time; this might reflect an under‐recruitment of critical areas during perception of emotional faces.
The MID task results suggest evidence of compensatory changes during adolescent development with increased prefrontal activation over time; this might allow cognitive control mechanisms to contextualise the PLE, so to prevent transition to clinically significant symptoms; an observation which is consistent with the aberrant salience model of psychosis.
My findings reinforce the role of prefrontal, limbic and striatal brain areas in the aetiology of psychosis, beyond the bounds of the illness phenotype and without the confounds of the impact of the illness or the use of antipsychotic medication.
Original languageEnglish
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Supervisors/Advisors
Award date2018

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